浙江医学
浙江醫學
절강의학
ZHEJIANG MEDICAL JOURNAL
2014年
12期
1053-1055,1075
,共4页
吡格列酮%非酒精性脂肪性肝病%大鼠%氧应激%血红蛋白氧合酶
吡格列酮%非酒精性脂肪性肝病%大鼠%氧應激%血紅蛋白氧閤酶
필격렬동%비주정성지방성간병%대서%양응격%혈홍단백양합매
Pioglitazone%Non- alcoholic fatty liver disease%Rats%Oxidative sress%Heme oxygenase- 1
目的：观察吡格列酮对高脂饮食诱导的非酒精性脂肪性肝病（NAFLD）大鼠肝脏组织氧化应激的影响。方法将30只SD大鼠随机分为正常组、模型组和吡格列酮组（每组10只）。正常组全程饲以普通饲料，另两组均给予高脂饮食。6周后每组各处死2只大鼠，验证NAFLD造模成功后，给予吡格列酮组大鼠10mg·kg-1·d-1吡格列酮灌胃，正常组、模型组给予相应体积的0.9%氯化钠溶液灌胃。6周后处死并留取肝组织，行病理组织学检查，硫代巴比妥酸法测定丙二醛（MDA）的含量，免疫组织化学法检测肝脏组织血红蛋白氧合酶（HO）-1的表达。结果与模型组相比，吡格列酮组大鼠肝组织病变改善，MDA的含量显著下降，且该组肝脏组织内HO-1表达较正常组、模型组均显著升高（均P＜0.05）。结论吡格列酮可诱导NAFLD大鼠肝脏组织内HO-1的表达，减弱氧化应激，可能是其改善NAFLD病理变化的机制之一。
目的：觀察吡格列酮對高脂飲食誘導的非酒精性脂肪性肝病（NAFLD）大鼠肝髒組織氧化應激的影響。方法將30隻SD大鼠隨機分為正常組、模型組和吡格列酮組（每組10隻）。正常組全程飼以普通飼料，另兩組均給予高脂飲食。6週後每組各處死2隻大鼠，驗證NAFLD造模成功後，給予吡格列酮組大鼠10mg·kg-1·d-1吡格列酮灌胃，正常組、模型組給予相應體積的0.9%氯化鈉溶液灌胃。6週後處死併留取肝組織，行病理組織學檢查，硫代巴比妥痠法測定丙二醛（MDA）的含量，免疫組織化學法檢測肝髒組織血紅蛋白氧閤酶（HO）-1的錶達。結果與模型組相比，吡格列酮組大鼠肝組織病變改善，MDA的含量顯著下降，且該組肝髒組織內HO-1錶達較正常組、模型組均顯著升高（均P＜0.05）。結論吡格列酮可誘導NAFLD大鼠肝髒組織內HO-1的錶達，減弱氧化應激，可能是其改善NAFLD病理變化的機製之一。
목적：관찰필격렬동대고지음식유도적비주정성지방성간병（NAFLD）대서간장조직양화응격적영향。방법장30지SD대서수궤분위정상조、모형조화필격렬동조（매조10지）。정상조전정사이보통사료，령량조균급여고지음식。6주후매조각처사2지대서，험증NAFLD조모성공후，급여필격렬동조대서10mg·kg-1·d-1필격렬동관위，정상조、모형조급여상응체적적0.9%록화납용액관위。6주후처사병류취간조직，행병리조직학검사，류대파비타산법측정병이철（MDA）적함량，면역조직화학법검측간장조직혈홍단백양합매（HO）-1적표체。결과여모형조상비，필격렬동조대서간조직병변개선，MDA적함량현저하강，차해조간장조직내HO-1표체교정상조、모형조균현저승고（균P＜0.05）。결론필격렬동가유도NAFLD대서간장조직내HO-1적표체，감약양화응격，가능시기개선NAFLD병리변화적궤제지일。
Objective To investigate the effects of pioglitazone on oxidative stress in rats with high fat diet- induced non- alcoholic fatty liver disease (NAFLD). Methods Thirty SD rats were randomly divided into normal group, model group and pioglitazone group (n=10 in each). NAFLS was induced by feeding of high- fat diet in rats of model and pioglitazone groups. Rats in pioglitazone group were gavaged with 10mg/kg of pioglitazone daily;rats in normal and model groups received an equal vol-ume of saline. Two rats from each group were sacrificed at the end of week 6 for pathological examination;and at the end of week 12 al rats were sacrificed. The histological examinations were performed, contents of malondialdehyde (MDA) and heme oxyge-nase- 1 (HO- 1) in liver were determined. Results Compared with model group, the degrees of hepatic steatosis and inflamma-tion were significantly al eviated and contents of MDA in liver were decreased in pioglitazone group(P<0.05). The liver HO- 1 lev-els were significantly higher in pioglitazone group than those in normal and model groups(P<0.05). Conclusion Pioglitazone can induce the expression of HO- 1 in liver, which is associated with its protective effect on oxidative stress and attenuation of non- alcoholic fatty liver disease in rats.
